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Hyperthyroid patients show an increase in heart rate throughout sleeping and waking hours, whereas in hypothyroid patients a decrease in basal, average, and maximal heart rates is found although most are not bradycardic (slow heartbeat) at rest. The biologically relevant TH, T3, exerts a direct effect on cardiac myocytes by binding to nuclear T3 receptors influencing cardiac gene expression. T3 increases the systolic depolarization and diastolic repolarization rate and decreases the action potential duration and the refraction period of the atrial myocardium as well as the atrial/ventricular nodal refraction period. The mechanism by which T3 induces the electrophysiological changes is related in part to its effects on sodium pump density and enhancement of Na+ and K+ permeability. Heart rate effects are mediated by T3-based increases in the pacemaker ion current in the sinoatrial node. The L-type calcium channel 1D, which also serves as an important pacemaker function, is also increased by T3. THs exert marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect).
Therefore, T3 markedly shortens diastolic relaxation, i.e., the hyperthyroid heart relaxes with a higher speed, whereas diastole is prolonged in hypothyroid states. Thyroid dysfunction alters blood pressure: hyperthyroidism has only minor effects on mean arterial blood pressure because increases in systolic pressure, caused by increased stroke volume, are offset by decreases in diastolic pressure, due to peripheral vasodilatation. Conversely, hypothyroidism is associated with increases in diastolic pressure.
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